0.05). CONCLUSIONS Proper use of disinfectants based on routine cleaning can achieve good results in the nosocomial infection control of the NICU.

AIM: To investigate the changes of the L-type calcium channel subunit expression and calcium currents (I_~Ca -L) in cultured rat ventricular myocytes infected by coxsackie virus B_3 (CVB_3). METHODS: Primary cultured neonatal rat ventricular myocytes were infected with CVB_3. The changes of L-type calcium channel subunits mRNA in normal and infected myocytes were measured by semi-quantitative reverse transcription-polymerase chain reaction. I_~Ca -L was recorded in two groups respectively using whole cell patch-clamp techniques. RESULTS: The expression of ?_1 and ? subunits of L-type calcium channel mRNA increased in the infected group compared with the normal one (4.00?0.07 vs 2.21?0.41, P0.05). The average current density of I_~Ca -L significantly increased by CVB_3 infection [(-8.66?0.99) pA/pF vs (-6.97?1.75) pA/pF, P

AIM:To study the influence of angiotensin Ⅱ(AngⅡ) on ATP-binding cassette transporter A1 in THP-1 derived foam cells.The variance of the expression of ABCA1,the content and the effluent rate of cholesterol were also investigated.METHODS: The regulatory effect of AngⅡ on the expression of ABCA1 mRNA and protein in THP-1 derived form cells were measured by RT-PCR and Western blotting.The effect of variance of cholesterol content was measured by zymochemistry via-fluorospectrophotometer,cholesterol effluent was measured by liquid scintillator.RESULTS: A positive facilitative effect of Ang Ⅱon form cells was observed.Total cholesterol content were increased significantly by Ang Ⅱ treatment(P

Objective To clone and sequence the partial gene of Schistosoma japonicum phosphoglycerate kinase (SjPGK). Methods A pair of primers were designed and synthesized according to the cDNA sequence of Schistosoma mansoni phosphoglycerate kinase (SmPGK) gene. The gene fragment of SjPGK was amplified and isolated from the total RNA of S.japonicum by reverse-transcription polymerase chain reaction (RT-PCR). The gene fragment was cloned into the cloning vector of pMD18-T, The positive clones were acquired and identified with restrictive enzymes and PCR amplification. After being sequenced with DNA auto-sequence analysis instrument,the cDNA sequence of SjPGK was searched for homologue identity with NCBI BLAST program. Results The gene encoding SjPGK was obtained and isolated by RT-PCR .The fragment of SjPGK was about 830 bp.The cDNA sequence of the phosphoglycerate kinase was highly homologous between Schistosoma mansoni and Schistosoma japonicum. The identity of nucleotide sequence was 85% and score 672, and the identity of amino sequence was 94% and score 473. Conclusion The partial gene of encoding SjPGK is cloned into the cloning vector of pMD18-T, which gives the basis for discovering new candidate vaccine molecular for schistosomiasis.

Microthrombosis may be involved in the pathogenesis of cardiac microangiopathy due to diabetes. Recent studies have shown that fibrinogen-like protein 2 (fgl2) plays a pivotal role in microthrombosis in viral hepatitis, acute vascular xenograft rejection and cytokine-induced fetal loss syndrome. The current study was designed to examine the expression of fgl2 in microvascular endothelial cells and investigate the effects of microthrombi due to fgl2 on cardiac function and structure in rats with type 2 diabetes. Following induction of type 2 diabetes, 24 rats were observed dynamically. Fgl2 expression and related cardiac microthrombosis were examined. Local or circulating TNF-α was measured. Coronary flow (CF) per min was calculated as an index of cardiac microcirculation. Cardiac function and morphology were evaluated. It was found that Fgl2 was highly expressed in cardiac microvascular endothelial cells of rats with type 2 diabetes, which was promoted by local or circulating TNF-α. The Fgl2 expression was associated with cardiac hyaline microthrombosis. In parallel with the fgl2 expression, CF per min, cardiac diastolic or systolic function and cardiac morphology were aggravated to some extent. It was concluded that in rats with type 2 diabetes, microthrombosis due to fgl2 contributes to the impairment of cardiac diastolic or systolic function and morphological changes.

BACKGROUND: T-type or linear type external fixator is applied in transcervical fracture in the elderly. Because its fixing force is weak, so it is difficult to avoid the aggravation of complication due to long term lay up in severe osteoporosis. Based on this reason,percutaneous penetrating arch tri-claw external fixator is designed to treat elderly transcervical fracture with strong fixing force for the realization of early restoration to the active status before injury to reduce complication.OBJECTIVE:To design pereutaneous penetrating arch tri-claw external fixator for the treatment of elderly transcervical fracture for the investigation of its feasibility.DESIGN: A self-controlled study by employing patients as subjects.SETTING: Department of orthopedic surgery of the first affiliated hospital of a universityPARTICIPANTS: Thirty-one cases of elderly transcervical fracture including 18 males and 13 females aged between 71 and 86 years old with an average age of 79 years were admitted by the Department of Orthopedics of the First Affiliated Hospital of Nanhua University between December 2002 and June 2004.METHODS: Percutaneous penetrating arch tri-claw external fixator was applied in the treatment of 31 cases with elderly transcervical fracture for the observation of its clinical effects, and the force-bearing situation and stability of the external fixator during application were analyzed by theoretical mechanics.MAIN OUTCOME MEASURES: ① The functional effects of percutaneous penetrating arch tri-claw external fixator applied in the therapy of transcervical fracture(sub-femoral head type,transcervical type and femoral basilar type); 2② The force-bearing situation and the stability of the fixing point on the fixator; ③ The restoration of activity in hip joint and fracture union time RESULTS: ① Patients could sit and stand immediately after the applicationof the fixator, and its fixing reinforce was analyzed by theoretic mechanics during standing(the force on upper fixing point A, B or C was 1/22, 1/2 or 1/2 of the lower fixing point) . The unidirectional flexion and extension activity of the hip joint overcame hip-inversion and rotational disposition at the distal end of the fracture. The hip-joint axial compression board caused compact embedment and insertion of the fracture end and vertical crush to simulate fracture union by stability and compressive strain. ② The stability of percutaneous penetrating arch tri-claw external fixator: No disposition was found during the application except rotational disposition during activity in sub-femoral head type fracture. The fixation was stable, the operative trauma was less,and the operation was simple with good accommodation. No complication was found due to long-term lay up and no re-disposition due to the loosening of the external fixator was found. ③ The hip-joint flexion-extension function was restored within 7 days averagely and fracture healing time was about 2 to 3 months, average of 2.4 months.CONCLUSION: No re-injury is found dter the application of percutaneous penetrating arch tri-claw external fixator, which has small force bearing at upper fixing point with strong stability. There is strain stimulation on the cross section of the fracture to promote fracture healing. The articular function status before injury could be restored at early stage.

AIM: To clarify the relationship between the cytokine and collagen in myocardial remodeling after acute myocardial infarction(MI) in rats.METHODS: In MI group,Wistar rats were undergone acute myocardial infarction by ligation of the anterior descending coronary artery.Sham operation was made in rats as control.The mRNA expression of collagen and cytokines such as TNF-? and TGF-?_1 in infract and non-infarct region of left myocardium were detected by RT-PCR at different time point(3 d,1 and 4 weeks).RESULTS: Collagen type Ⅰ and Ⅲ elevated as well as the TNF-? and TGF-?_1 in the MI group at 3th day.Expression of collagen type Ⅰ and Ⅲ were higher in the infarct region than that in the non-infarct region even at 4 weeks.TNF-? and TGF-?_1 peaked at 1 week and declined gradually to the baseline,which was still higher than those in control group(P

Objective To evaluate the role of the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)or Janus kinase(JAK)/signal transducer and activator of transcription 3(STAT-3)signaling pathways in reduction of myocardial ischemia-reperfusion(I/R)injury by combination of limb ischemic and morphine postconditioning in rats.Methods Eighty SPF healthy male Sprague-Dawley rats,aged 8 weeks,weighing 280-320 g,were used in the study.Myocardial I/R was induced by occlusion of the left anterior descending branch of the coronary artery for 30 min followed by 120 min reperfusion.The rats were divided into 8 groups(n=10 each)using a random number table:I/R group,limb ischemic postconditioning group(LIP group),morphine postconditioning group(group MP),combination of limb ischemic and morphine postconditioning group(LIP+MP group)and signaling pathway blocker groups(I/Rb group,LIPb group,MPb group,LIP+MPb group).In I/R,LIP,MP and LIP+MP groups,the animals were sacrificed at the end of reperfusion,and myocardial specimens in ischemic and non-ischemic regions were obtained for determination of phosphorylated STAT-3(p-STAT-3),STAT-3,phosphorylated Akt(p-Akt)and Akt expression(by Western blot)and STAT-3 and Akt mRNA expression(by polymerase chain reaction).In I/Rb,LIPb,MPb and LIP+MPb groups,PI3K/Akt signaling pathway blocker LY294002 0.3 mg/kg was intravenously injected in 5 rats of each group,and JAK/STAT-3 signaling pathway blocker AG490 5 mg/kg was intravenously injected in the other 5 rats of each group.The animals were sacrificed at the end of reperfusion,and myocardial specimens in the ischemic region were obtained for determination of myocardial infarct size.Results Compared with I/R group,the p-STAT-3/STAT-3 ratio in LIP,MP and LIP+MP groups and p-Akt/Akt ratio in LIP+MP group were significantly increased,and the expression of STAT-3 and Akt mRNA was up-regulated in LIP+MP group(P<0.05).Compared with LIP and MP groups,the p-STAT-3/STAT-3 and p-Akt/Akt ratios were significantly increased,and the expression of STAT-3 and Akt mRNA was up-regulated in LIP+MP group(P<0.05).There was no significant difference in myocardial infarct size between the four groups when PI3K inhibitor LY294002 was applied(P>0.05).When JAK2 inhibitor AG490 was applied,the myocardial infarct size was significantly smaller in LIP+MPb group than in I/Rb,LIPb and MPb groups(P<0.05),and there was no significant difference in myocardial infarct size between I/Rb,LIPb and MPb groups(P>0.05).Conclusion Combination of limb ischemic and morphine postconditioning can enhance the activation of PI3K/Akt or JAK/STAT-3 signaling pathways,and the cardioprotection is dependent on the integrity of the PI3K/Akt signaling pathway and partially dependent on the integrity of the JAK/STAT-3 signaling pathway when applied in combination in rats.

To observe the dynamic changes of the TGF-beta1 expressed in the infarct and non-infarcted region of rat heart during the ventricular remodeling (day 3, 7, 28, 180), myocardial infarction rat model was made and relationship between the cytokine and indicator of myocardial remodeling was analyzed. After the detection of hemodynamic parameter was performed by the Powerlab devices, the size of myocardial infarction and the morphology change was detected by TTC and HE, respectively. The relative levels of mRNA of TGF- beta1, collagen type I, III, and fetal gene beta-MHC were detected by RT-PCR. The distribution of TGF- beta1 protein in the myocardium was detected by immunohistochemistry. The results showed that the size of infarction was higher than that of the sham operated groups in the infarcted group (44.5 +/- 0.5 vs 0). The difference in hemodynamic parameters between the infarcted group and sham operated group was significant (P < 0.01). HE staining showed that inflammatory cells were accumulated in the infarcted region at the beginning of the 3rd day, which lasted 4 weeks. Then, it decreased gradually. beta-MHC in the non-infarcted region rose from the 3rd day, reaching its peak at the 4th week, and it decreased gradually. The ratio of the collagen type I/III showed similar changes as compared with the sham operated groups (P < 0.01). And the relative mRNA levels in the non-infarcted group were significantly higher than that in the infarcted and sham operated group (P < 0.01) at day 180. Linear regression analysis indicated that the TGF-beta1 was positively correlated with the ventricular remodeling. It was concluded that the cytokine TGF-beta1 participates in the process of the myocardial remodeling, which could be a strategy in the interference of myocardial remodeling.

Microthrombosis may be involved in the pathogenesis of cardiac microangiopathy due to diabetes. Recent studies have shown that fibrinogen-like protein 2 (fgl2) plays a pivotal role in microthrombosis in viral hepatitis, acute vascular xenograft rejection and cytokine-induced fetal loss syndrome. The current study was designed to examine the expression of fgl2 in microvascular endothelial cells and investigate the effects of microthrombi due to fgl2 on cardiac function and structure in rats with type 2 diabetes. Following induction of type 2 diabetes, 24 rats were observed dynamically. Fgl2 expression and related cardiac microthrombosis were examined. Local or circulating TNF-a was measured. Coronary flow (CF) per min was calculated as an index of cardiac microcirculation. Cardiac function and morphology were evaluated. It was found that Fgl2 was highly expressed in cardiac microvascular endothelial cells of rats with type 2 diabetes, which was promoted by local or circulating TNF-α. The Fgl2 expression was associated with cardiac hyaline microthrombosis. In parallel with the fgl2 expression, CF per min, cardiac diastolic or systolic function and cardiac morphology were aggravated to some extent. It was concluded that in rats with type 2 diabetes, microthrombosis due to fgl2 contributes to the impairment of cardiac diastolic or systolic function and morphological changes.